Breast cancer risk in women is markedly reduced by an early pregnancy and lactation. Using an experimental model we have demonstrated that the susceptibility of rats to carcinogenesis decreases with aging and is nullified when pregnancy and lactation occur prior to carcinogen administration. We have shown that the susceptibility of the mammary gland to carcinogenesis is influenced by variables such as the degree of differentiation of the gland, rate of DNA synthesis and cell proliferation, and variations in cell kinetics. The above mentioned facts were substantiated by determining the length of the cell cycle (Tc) and of each of the cell cycle phases, and the growth fraction (GF) of the epithelial cells lining the mammary gland structures. Our results indicate that in the mammary gland of young virgin rats the various structures developed as a consequence of progressive differentiation of the gland, have markedly different GF, which is highest in the least differentiated structure, the TEB, decreasing progressively in the more differentiated structures, TD and AB. The more undifferentiated structures have a shorter Tc, while in the more differentiated ones a progressive lengthening of Tc, due mainly to a lengthening of G1, is observed. These differences between the more differentiated and the undifferentiated are accentuated with aging. Complete differentiation of the mammary gland as a consequence of pregnancy and lactation eliminates the undifferentiated structures, with a concomitant decrease in GF and more marked lengthening of Tc. Pregnancy induces in the mammary gland two basic changes in cell kinetic parameters: one of them is the increase in the size of the Go compartment, and the second change is the lengthening of Tc at the expense of G1. Our next objective is to determine whether these differences in cell kinetics are associated with a different DNA-repair capacity of the cell in susceptible and net-susceptible animals.